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Serotonin

Migraines are intricate neurological conditions characterized by headaches, light and sound sensitivity, nausea, and cognitive issues. Studies indicate that serotonin (5-HT) significantly contributes to the onset of migraines.

How Serotonin Influences Migraines

Serotonin plays a crucial role in managing pain, blood vessel activity, and inflammation within the brain. Fluctuations in serotonin levels can instigate migraines through various pathways:

Serotonin Levels Decline Prior to a Migraine Attack

• Typically, serotonin aids in constricting blood vessels.

• However, just before a migraine strikes, serotonin levels decrease, resulting in the dilation of blood vessels, which leads to pain and inflammation.

Serotonin Impacts Pain Sensitivity

• Reduced serotonin heightens the nervous system's sensitivity to pain.

• This accounts for the fact that individuals suffering from migraines frequently endure more severe pain compared to others.

Serotonin Imbalance Provokes Inflammation

• A deficiency in serotonin amplifies inflammation in the brain, exacerbating migraine symptoms.

Serotonin Governs Sleep and Mood

• Insufficient serotonin can result in sleep issues, depression, and anxiety, all of which are associated with an increased frequency of migraines.

Noradrenaline

Noradrenaline functions as both a hormone and a neurotransmitter that plays a crucial role in the fight-or-flight response. It is synthesized in the brainstem, particularly in the locus coeruleus, as well as in the adrenal glands. This compound influences various bodily functions, including blood vessel constriction, heart rate, sleep-wake cycles, and the perception of pain.

How Noradrenaline Relates to Migraines

Pain Modulation

Noradrenaline plays a key role in modulating pain via descending pain-inhibitory pathways located in the brainstem.

When noradrenaline activity is low, the effectiveness of these inhibitory pathways may diminish, leading to increased pain sensitivity during migraine episodes.

Low initiative, even for activities you find enjoyable.

Struggles with maintaining focus or completing tasks.

A pervasive feeling of “why bother?”

Vascular Effects

Migraines, especially those accompanied by aura, are associated with alterations in cerebral blood flow.

Noradrenaline induces vasoconstriction, which is the narrowing of blood vessels. An imbalance in noradrenaline levels could result in abnormal vascular responses, potentially triggering or exacerbating migraines.

Stress and Cortisol Link

Stress is a well-known trigger for migraines, and noradrenaline serves as a primary chemical involved in the stress response.

Chronic stress can lead to elevated levels of noradrenaline, which may sensitize neurons, heighten inflammation, and contribute to central sensitization, a significant characteristic of chronic migraines.

Sleep and Wakefulness

Noradrenaline is vital for the regulation of REM sleep and maintaining alertness.

Disrupted sleep patterns or poor sleep quality are recognized triggers for migraines, likely due to an imbalance in noradrenaline levels.

Trigeminal Nerve Interaction

The trigeminal nerve plays a significant role in the experience of migraine pain.

Noradrenaline affects this system and can either reduce or enhance nociceptive (pain) signals, depending on which receptor subtypes are activated.

Migraines are not merely intense headaches; they are intricate neurological occurrences often influenced by hormonal fluctuations. If you suffer from chronic migraines, when these hormones become unbalanced, your brain's sensitivity to pain, light, sound, and stress increases—setting the stage for migraines.

Adrenaline

Adrenaline acts as your body's emergency response mechanism. It enables you to cope with stress, but an excess or deficiency can have adverse effects—particularly on your brain.

In Migraine:

• Surges of adrenaline frequently initiate migraine attacks—especially following emotional stress or missed meals.

• As adrenaline levels decrease, blood vessels expand, resulting in throbbing pain and exhaustion.

Common Patterns:

• Migraine following arguments or stress

• Throbbing pain in the temples or behind the eyes

• Cold hands, rapid heartbeat, and restlessness prior to an attack

GABA: Your Brain’s Off Switch

GABA serves as the calming neurotransmitter that aids your brain in slowing down, resting, and recuperating.

In Migraine:

• Insufficient GABA levels render your brain overly reactive to light, sound, and sensory stimuli.

• This also disrupts sleep quality, complicating recovery from migraines.

Common Patterns:

• Auras or visual disturbances preceding a migraine

• Poor sleep quality before or after attacks

• Increased anxiety or sensory overload

Glutamate

Glutamate is the primary excitatory neurotransmitter in the brain—it energizes neuron activity and is crucial for pain perception, sensory processing, and vasodilation (the widening of blood vessels).

Glutamate's Role in Migraine

Inducing Cortical Spreading Depression (CSD)

• CSD represents a wave of hyperactive neurons followed by a shutdown that propagates across the brain cortex—this is a fundamental mechanism behind aura in migraines.

• Excess glutamate induces CSD by overstimulating neurons, rendering the brain hyperexcitable and susceptible to migraine onset.

Sensory Overload & Pain Amplification

Sensory Overload & Pain Amplification

• The trigeminal nerve pathways (the pain highway for the face/head)

• The cortex and thalamus (sensory relay centers)

This results in:

• Sensitivity to light, sound, and smell (photophobia, phonophobia)

• Pulsating pain and feelings of nausea

• Aura symptoms affecting visual or sensory systems

Glutamate and Chronic Migraine

Research indicates that individuals suffering from chronic or frequent migraines have consistently high levels of glutamate in their cerebrospinal fluid and blood.

This ongoing glutamate surplus results in:

• A reduced threshold for migraines

• More frequent episodes

• A higher chance of moving from episodic to chronic migraine